Mediation of Ventilatory Adaptations.

Dempsey, J A; Forster, H. V.

doi:10.1152/physrev.1982.62.1.262

Cited by 289 publications

(162 citation statements)

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“…The coordinated response of central and peripheral chemoreceptors to hypercapnia, which increases arterial P CO 2 (Pa CO 2 ) and decreases arterial pH (pHa), generally increases ventilation (Milsom, 2002). The magnitude of the ventilatory response to hypercapnia often decreases with time, which may reflect independent effects of Pa CO 2 and pHa on breathing (Dempsey and Forster, 1982). For example, in male pekin ducks breathing 5% CO 2 , the immediate increase in total ventilation diminishes over time, which occurs in conjunction with a partial recovery of pHa (Dodd and Milsom, 1987).…”

Section: Introductionmentioning

confidence: 99%

Ventilatory roll off during sustained hypercapnia is gender specific in pekin ducks

Dodd

Scott

Milsom

2007

Respiratory Physiology & Neurobiology

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The objective of the present study was to examine the relative roles of peripheral versus central mechanisms in producing ventilatory adjustments in pekin ducks during prolonged (5 h) hypercapnia (5% inspired CO 2 ), and to determine whether these adjustments differed between male and female ducks. After 20 min of CO 2 exposure, intact ducks increased total ventilation (V E ) 2.5-3-fold above control values, due to large increases (∼200%) in tidal volume (V T ) and slightly smaller increases (∼140%) in breathing frequency (f R ). This response was accompanied by respiratory acidosis (pHa fell from ∼7.46 to ∼7.41) and hypercapnia (Pa CO 2 increased from ∼35 to ∼40 Torr). In males,V E fell progressively thereafter due exclusively to a fall in f R , in parallel with a rapid partial recovery of pH (to 7.44) while Pa CO 2 continued to climb (to ∼42 Torr). In females,V E remained elevated during hypercapnia, and no pH recovery occurred. This suggests that a respiratory decline resulting from acid-base compensation (probably due to HCO 3 − mobilization) occurred in males but not in females. Bicarbonate mobilization, and thus pH compensation, may have been reduced in females due to the CaCO 3 requirements of eggshell formation. In males, the acute ventilatory response was reduced slightly by denervation of the carotid bodies or intrapulmonary chemoreceptors, but there was no effect of denervation of either receptor group on the responses to prolonged CO 2 . We conclude that pH compensation triggered by constant or increasing Pa CO 2 , acting at central chemoreceptors, likely mediates the respiratory adjustments seen in male pekin ducks during hypercapnia. Furthermore, we suggest that this ventilatory response be considered a gender-specific hypercapnic ventilatory roll off, in the context of the various time domains of the hypercapnic ventilatory response.

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Section: Introductionmentioning

confidence: 99%

Ventilatory roll off during sustained hypercapnia is gender specific in pekin ducks

Dodd

Scott

Milsom

2007

Respiratory Physiology & Neurobiology

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“…Our studies, which examined the direct effects of nicotine on CB chemoreceptors in vitro, also indicated a marked elevation in released DA. However, this response appeared to involve multiple factors, some of which may underlie the "blunting" effect of sustained hypoxia on the CB ventilatory response in the neonatal period (Dempsey and Forster, 1982;Eden and Hanson, 1987). In particular, our studies suggest that chronic nicotine may cause elevation in extracellular DA by inhibiting the activity of the DA transporter and regulation of nAChRs on chemoreceptor cells.…”

Section: Discussionmentioning

confidence: 67%

Role of Acetylcholine Receptors and Dopamine Transporter in Regulation of Extracellular Dopamine in Rat Carotid Body Cultures Grown in Chronic Hypoxia or Nicotine

Jackson

Nurse

1998

Journal of Neurochemistry

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Using dissociated rat carotid body (CB) cultures, we compared levels of extracellular dopamine (DA) around oxygen-sensitive glomus cells grown for -~12 days in normoxia (Nox; 20% 02), chronic hypoxia (CHox; 6% 02), or chronic nicotine (CNic; 10~tMnicotine, 20% 02), with or without acetylcholine (ACh) receptor (AChR) agonists/antagonists and blockers of DA uptake. In Nox cultures, extracellular DA, determined by HPLC and normalized to the number of tyrosine hydroxylase-positive glomus cells present, was augmented by acute (-.15-mm) exposure to hypoxia (5% 02;~-~6x basal), high extracellular K~(30 mM; --lOx basal), nomifensine (1 1.sM; a selective DA uptake inhibitor; --.3x basal), and nicotine (100~sM; --5x basal), but not methylcholine (300 1zM; a specific muscarinic agonist). In contrast, in CHox cultures where basal DA release is markedly elevated (--9x control), the stimulatory effect of high K~(3-4x basal) and acute hypoxia (--2x basal) on DA release persisted, but nicotine and nomifensine were no longer effective and methylcholine had a partial inhibitory effect. In CNic cultures, basal DA levels were also elevated (-~9xcontrol), similar to that in CHox cultures; however, although acute hypoxia had a stimulatory effect on DA release (.-2x basal), nicotine, nomifensine, and high K~were ineffective. The elevated basal DA in both CHox and CNic cultures was attenuated by acute or chronic treatment with mecamylamine (100~sfl~, a nicotinic AChR (nAChR) antagonist. In addition, long-term (16-h), but not acute (15-mm), treatment with the muscarinic antagonist atropine (1~M)produced an additional enhancement of basal DA levels in CHox cultures. Thus, after chronic hypoxia or nicotine in vitro, extracellular DA levels around CB chemoreceptor cell clusters appear to be set by a variety of factors including released ACh, positive and negative feedback regulation via nAChRs and muscarinic AChRs, respectively, and modulation of DA transporters. These results provide insight into roles of endogenous transmitters in the adaptation of CB chemoreceptors to chronic hypoxia and suggest pathways by which neuroactive drugs, e.g., nicotine, can interfere with the protective chemoreflex response against hypoxia. Key Words: Dopamine uptake-Glomus cell culture-Nicotinic and muscarinic acetylcholine receptors-a2 chemoreceptors-HPLC.

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“…However, our laboratory and others have shown that these effects do not persist into adulthood (9,13), and the HCVR may normalize after only 2 wk of normocapnic recovery (9). Thus there are no apparent differences between the transient blunting of the HCVR following neonatal hypercapnia and the ventilatory acclimation to chronic hypercapnia in adult rats and other mammals (23). Intermittent hypercapnia (0 or 7.5% CO 2 at 1-h intervals) for the first 2 postnatal wk has no effect on the HCVR at either 2 or 7 wk of age in rats (K. E. R. Russell, J.C. Simons, and R. W. Bavis, unpublished observations); the adult HVR is also unchanged following this intermittent hypercapnia protocol (10).…”

Section: Developmental Plasticity In Respiratory Control: Examplesmentioning

confidence: 73%

Long-term effects of the perinatal environment on respiratory control

Bavis¹,

Mitchell²

2008

Journal of Applied Physiology

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The respiratory control system exhibits considerable plasticity, similar to other regions of the nervous system. Plasticity is a persistent change in system behavior triggered by experiences such as changes in neural activity, hypoxia, and/or disease/injury. Although plasticity is observed in animals of all ages, some forms of plasticity appear to be unique to development (i.e., “developmental plasticity”). Developmental plasticity is an alteration in respiratory control induced by experiences during “critical” developmental periods; similar experiences outside the critical period will have little or no lasting effect. Thus complementary experiments on both mature and developing animals are generally needed to verify that the observed plasticity is unique to development. Frequently studied models of developmental plasticity in respiratory control include developmental manipulations of respiratory gas concentrations (O2 and CO2). Environmental factors not specifically associated with breathing may also trigger developmental plasticity, however, including psychological stress or chemicals associated with maternal habits (e.g., nicotine, cocaine). Despite rapid advances in describing models of developmental plasticity in breathing, our understanding of fundamental mechanisms giving rise to such plasticity is poor; mechanistic studies of developmental plasticity are of considerable importance. Developmental plasticity may enable organisms to “fine tune” their phenotype to optimize the performance of this critical homeostatic regulatory system. On the other hand, developmental plasticity could also increase the risk of disease later in life. Future directions for studies concerning the mechanisms and functional implications of developmental plasticity in respiratory motor control are discussed.

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Mediation of Ventilatory Adaptations.

Cited by 289 publications

References 0 publications

Ventilatory roll off during sustained hypercapnia is gender specific in pekin ducks

Ventilatory roll off during sustained hypercapnia is gender specific in pekin ducks

Role of Acetylcholine Receptors and Dopamine Transporter in Regulation of Extracellular Dopamine in Rat Carotid Body Cultures Grown in Chronic Hypoxia or Nicotine

Long-term effects of the perinatal environment on respiratory control

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